Urinary kallikrein and kinin and plasma bradykinin were measured in normal subjects and in patients with hypertension, Bartter' syndrome, and scleroderma on controlled intakes of sodium and potassium. Plasma bradykinin in normal subjects is responsive to changes in posture and sodium intake and parallels changes in the renin-angiotensin-aldosterone system. Urinary kallikrein increases with sodium restriction but urinary kinin excretion is unchanged. Urinary kinin excretion is significantly correlated with kallikrein excretion on 109 meq sodium intake but not on 9 meq sodium intake. This suggests that urinary kallikrein is not the only determinant of urinary kinin excretion. Patients with Bartter's syndrome have significantly elevated basal urinary kallikrein and plasma bradykinin but subnormal urinary kinin excretion. During prostaglandin synthetase inhibition urinary kallikrein and plasma bradykinin decreased while urinary kinin excretion increased toward normal. These data indicate an involvement of the kallikrein-kinin system in this syndrome and its relationship to other vasoactive systems. Patients with scleroderma but without hypertension or apparent renal disease have subnormal urinary kallikrein excretion which may be related to reduced renal blood flow in these patients.